ArticleNucleic acids research2025
The Vsr-like protein FASTKD4 regulates the stability and polyadenylation of the MT-ND3 mRNA.
Article in Nucleic acids research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Human FASTK preferentially binds single-stranded and G-rich RNA.The FEBS journal · 2026Article
- FASTK post-transcriptional regulators - a 'FAST-tracK' in mitochondrial gene expression.Biochemical Society transactions · 2025Review
- FASTKD5 processes mitochondrial pre-mRNAs at noncanonical cleavage sites.Nucleic acids research · 2025Article
- Bi-allelic mutations in FASTKD5 are associated with cytochrome c oxidase deficiency and early- to late-onset Leigh syndrome.American journal of human genetics · 2025Article
- hnRNPH1: A Multifaceted Regulator in RNA Processing and Disease Pathogenesis.International journal of molecular sciences · 2025Review
- Identification and verification of mitochondria-related genes biomarkers associated with immune infiltration for COPD using WGCNA and machine learning algorithms.Scientific reports · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
Expression of the compact mitochondrial genome is regulated by nuclear encoded, mitochondrially localized RNA-binding proteins (RBPs). RBPs regulate the lifecycles of mitochondrial RNAs from transcription to degradation by mediating RNA processing, maturation, stability and translation. The Fas-activated serine/threonine kinase (FASTK) family of RBPs has been shown to regulate and fine-tune discrete aspects of mitochondrial gene expression. Although the roles of specific targets of FASTK proteins have been elucidated, the molecular mechanisms of FASTK proteins in mitochondrial RNA metabolism remain unclear. Therefore, we resolved the structure of FASTKD4 at atomic level that includes the RAP domain and the two FAST motifs, creating a positively charged cavity resembling that of the very short patch repair endonuclease. Our biochemical studies show that FASTKD4 binds the canonical poly(A) tail of MT-ND3 enabling its maturation and translation. The in vitro role of FASTKD4 is consistent with its loss in cells that results in decreased MT-ND3 polyadenylation, which destabilizes this messenger RNA in mitochondria.
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